The events of 9/11 sparked a revitalization of civil defense in the U.S. for emergency planning and preparedness for future radiological or nuclear event scenarios and specifically for mass casualty medical management of radiation exposure and injury. Research in medical countermeasure development in the form of novel pharmaceuticals to treat radiation injury and new radiation biodosimetry diagnostics, primarily focused on development of research models of uniform total-body irradiation (TBI). With the success of those models, it was recognized that most radiation exposures in the field will involve non-uniform heterogeneous irradiations and many partial-body or organ-specific irradiation models have been utilized. This review examines partial-body models of irradiations developed in the last decade for heterogeneous radiation exposures and organ-specific radiation exposure patterns. These research models have been used to further our understanding of radiation injury, novel medical countermeasures and biodosimetry diagnostics in development for future radiological and nuclear event scenarios.

This study explores the potential protective effects and mechanisms of astragaloside (AST) on microwave radiation-induced cardiac injury. Rats and H9c2 cells were irradiated with S-band microwave to induce in vivo and in vitro cardiac injury models. In irradiated rats, experiments such as electrophysiological examination, serum biochemical analysis, hematoxylin and eosin (H&E) staining, transmission electron microscopy (TEM), western blot, and immunohistochemical staining were performed after AST were administrated for 7 and/or 14 days. In irradiated H9c2 cells that were pretreated with 1-Azakenpaullone (glycogen synthase kinase-3b inhibitor) or AST, experiments such as TEM, cell counting kit-8 assay, western blot, tetramethylrhodamine methylester staining, and determination of reactive oxygen species (ROS), adenosine triphosphate (ATP) and mitochondrial membrane potential (MMP) were performed. In vivo results showed that at 7 days after exposure, microwave radiation-induced severe cardiac injury (as evidenced by abnormal electrocardiograms and cardiac tissue structure, increased serum myocardial enzyme activities and Ca²¹ concentration) and lower level of phosphorylation of glycogen synthase kinase-3b (p-GSK-3b^Ser9). All these changes were reversed after AST treatment. The results of in vitro experiments showed that microwave radiation induced a lower level of p-GSK-3b^Ser9, more mitochondrial permeability transition pore (mPTP) opening and more serious mitochondrial dysfunction (characterized by increased intracellular ROS production, decreased intracellular ATP synthesis and MMP decline) in H9c2 cells. All these changes were reversed by 1-Azakenpaullone and AST pretreatment. The findings suggest that AST could shield against microwave radiation-induced cardiac injury by promoting the phosphorylation of GSK-3b^Ser9, thereby inhibiting mPTP opening and restoring mitochondrial function. This study offers valuable insights into potential therapeutic strategies for mitigating the adverse effects of microwave radiation on cardiac health.

Past and current estimates of relative biological effectiveness (RBE) from the cohort analyses of atomic bomb survivors suggested not only that RBE may be much higher than those assessed by the United Nations Scientific Committee on Effects of Atomic Radiation (UNSCEAR) and International Commission on Radiological Protection (ICRP), but also that RBE may differ by organ and organ depth. This is at least partly due to how the ratio of neutron to gamma-ray dose changes with organ depth because of the more rapid attenuation of neutrons in tissue. Additionally, the RBE estimates from Life Span Study (LSS) data depend on the total dose and the neutron/gamma ratio. To further examine this issue, we calculated the mean quality factor based on Linear Energy Transfer (LET) distributions for representative organs and exposure scenarios of A-bomb survivors using Particle and Heavy Ion Transport code System (PHITS) simulation and the radiation quality factor [Q(L) relationship] defined by ICRP, as well as the Quality Factor (QF) function defined by the National Aeronautics and Space Administration (NASA). This is done in the context of the adult male phantom of the J45 series, which was created to precisely reproduce the anatomy of the Japanese population in 1945. We also investigate the depth dependence of the mean quality factors in the International Commission on Radiation Units and Measurements (ICRU) sphere irradiated by mono-energetic neutrons. Both the results from the human phantom, and from the ICRU sphere phantom suggest that the mean quality factors are approximately 15 and independent of the organ type, body depth, city and ground range when the contributions from the secondary c rays are excluded from the neutron doses. We also discuss reasons that RBE estimates from cohort analyses are generally much larger than those based on the mean quality factors.

Galactic cosmic rays (GCR) are among the biggest hindrances to crewed space exploration. The ions contributing the most to fluence and absorbed dose in free space are ¹H and ⁴He. In addition, their contribution to dose equivalent increases behind thick shields. In this work, the results of depth-dose measurements performed with high-energy ¹H and ⁴He ions (2 GeV and 480 MeV ¹H, and 430 MeV/u ⁴He) in structural (aluminum alloy), standard (PMMA and high-density polyethylene), innovative (lithium hydride) and in situ (Moon regolith simulant) shielding materials are presented. A strong dose build-up effect, due to target fragments and secondary protons, is observed in the first part of the Bragg curve for all the tested ion beams. The experimental results are compared to the Monte Carlo simulation tools most used for radiation protection in space, i.e., different physics lists of Geant4, PHITS, and FLUKA.

Lifetime risk estimates play a key role in many areas of radiation research. Here, the focus is on the lifetime excess absolute risk (LEAR) for dying from lung cancer due to occupational radon exposure based on uranium miners cohort studies. The major components in estimating LEAR were systematically varied to investigate the variability and uncertainties of results. Major components of the LEAR calculation are baseline mortality rates for lung cancer and all causes of death, risk model and exposure scenario. Sex-averaged mortality rates were chosen from a mixed Euro-American-Asian population, in addition to mortality rates to represent heavy and light smokers. Seven radon-related lung cancer risk models derived from different uranium miners cohorts were compared. As exposure scenarios, occupational exposure of two working level months (WLM) from age 18–64 years was considered, and three scenarios from the German uranium miners cohort. Further components were modified in sensitivity analyses. The LEAR was compared to other lifetime risk measures. With a range from less than 0.6 × 10^–4 to over 8.0 × 10^–4, LEAR per WLM estimates were influenced heavily by the choice of risk models. Notably, mortality rates, particularly lung cancer mortality rates, had a strong impact on LEAR per WLM across all models. The LEAR per WLM exhibited only low variation to changes in exposure scenarios for all risk models, except for the BEIR VI model fitted on the pooled 11 miners study. All assessed lifetime risk measures displayed a monotonically increasing relationship between exposure and lifetime risk at low to moderate exposures, with minor differences between ELR, REID, and LEAR (all per WLM). RADS yields the largest lifetime risk estimates in most situations. There is substantial variation in LEAR per WLM estimates depending on the choice of underlying calculation components. Reference populations and mortality rates should be selected with care depending on the application of lifetime risk calculations. The explicit choice of the lifetime risk measure was found to be negligible. These findings should be taken into consideration when using lifetime risk measures for radiation protection policy purposes.

The objective of this study was to investigate the relationship between radiotherapy sensitivity, glutamine synthetase (GS), and oxidative stress (OS) in human hepatocellular carcinoma (HCC) cells. HCC cells were X-ray irradiated, and the effect of glutamine synthetase inhibition on the proliferative capacity of HCC cells was examined using the CCK-8 colony formation assay. Real-time quantitative PCR assays were used to detect the effect of L-methionine sulfoximine (MSO) on cellular glutamine synthetase expression levels and the efficiency of glutamine synthetase knockdown in HepG2 cells. Glutamine synthetase activity assay kit was used to detect the viability of glutamine synthetase in cells and tissues. Oxidative stress production was assayed using an oxidative stress assay kit. Subcutaneous xenografts were used to detect the effects of L-methionine sulfoximine and radiation on tumor growth in vivo. The results showed that the apparent cell proliferation capacity of HCC cells after glutamine synthetase inhibition was significantly reduced after radiotherapy, which was closely related to the increased production of oxidative stress after radiotherapy. Furthermore, the results of animal experiments also showed that the combination of L-methionine sulfoximine and radiation induced a stronger tumor suppressive effect and that L-methionine sulfoximine could act as a radiosensitizer after radiotherapy.